Concept 1:
The core mechanism of respirophasic alterations of IVC diameter is its relationship with (actual, not transmural) CVP.
⬇️CVP -->⬆️venous return -->⬇️pressure within the IVC --> tendency to collapse (& vice versa).
Concept 2:
The IVC pressure-diameter relationship
##IVC evaluation in a spontaneously breathing patient -
Inspiration --> ⬇️ITP --> ⬇️CVP --> ⬇️IVC diameter (IVC collapses)
Say CVP reduces by 5 mmHg upon inspiration. Note that the effect on IVC diameter (collapsibility) would be much greater if baseline CVP is lower.
##IVC evaluation in a passive MV patient-
In passive PPV (i.e. no patient efforts e.g. paralyzed):
Inspiration --> ⬆️ITP --> ⬆️CVP --> ⬆️IVC diameter (IVC distends)
Again, the degree of IVC distension will depend on the CVP that would affect how full it is at baseline.
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Curiously, as opposed to IVC collapsibility (in NPV), IVC distensibility (in PPV) has NOT shown good correlation with baseline CVP (but very limited data: PMID: 1466886)
However, IVC distensibility HAS shown to predict fluid responsiveness in highly standardized conditions:
These include (i)Passive PPV (ii)TV - 8-12 cc/kg (iii)No cor pulmonale
A distensible IVC is interpreted as evidence of "preload reserve"
But note these are all indirect predictors of fluid responsiveness & in my mind, inferior in principle to direct predictors such as PLR
##IVC evaluation in patient-triggered PPV -
This scenario is much more common and rather complex. Patients often have alternating patient-triggered and machine-triggered breaths..
In a patient-triggered breath, there is an initial dip in ITP as the patient triggers.
This includes⬆️abdominal pressure with PPV (see Jon Emile's articles on PulmCCM)
Summary -
-NPV: IVC collapsibility is most helpful in estimating CVP
-Passive PPV: IVC distensibility can predict FR
-Patient-triggered PPV - IVC may collapse but use caution in interpreting.